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论文题目: Two-layer regulation of PAQR3 on ATG14-linked class III PtdIns3K activation upon glucose starvation
英文论文题目: Two-layer regulation of PAQR3 on ATG14-linked class III PtdIns3K activation upon glucose starvation
第一作者: Xu, DQ; Wang, Z; Chen, Y
英文第一作者: Xu, DQ; Wang, Z; Chen, Y
联系作者: Chen, Y (reprint author), 320 Yueyang Rd, Shanghai, Peoples R China.
英文联系作者: Chen, Y (reprint author), 320 Yueyang Rd, Shanghai, Peoples R China.
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发表年度: 2016
卷: 12
期: 6
页码: 1047-1048
摘要: As a central node of the macroautophagy/autophagy process, the BECN1/Beclin1-PIK3C3/VPS34 complex participates in different steps of autophagy by interactingwithmultiplemolecules. The ATG14-associated PIK3C3 complex is involved in autophagy initiation, whereas the UVRAG-associated complex mainly modulates autophagosome maturation and endosome fusion. However, the molecular mechanism that coordinates the sequential execution of the autophagy program remains unknown. We have recently discovered that a Golgi-resident protein, PAQR3, regulates autophagy initiation as it preferentially facilitates the formation of the ATG14-linked PIK3C3 complex instead of the UVRAG-associated complex. Upon glucose starvation, AMPK directly phosphorylates T32 of PAQR3, which is crucial for the activation of the ATG14-associated class III PtdIns3K. Furthermore, Paqr3-deleted mice have a deficiency in exercise-induced autophagy as well as behavioral disorders. Thus, this work not only uncovers the regulatory mechanism of PAQR3 on autophagy initiation, but also provides a potential candidate therapeutic target for neurodegenerative diseases.
英文摘要: As a central node of the macroautophagy/autophagy process, the BECN1/Beclin1-PIK3C3/VPS34 complex participates in different steps of autophagy by interactingwithmultiplemolecules. The ATG14-associated PIK3C3 complex is involved in autophagy initiation, whereas the UVRAG-associated complex mainly modulates autophagosome maturation and endosome fusion. However, the molecular mechanism that coordinates the sequential execution of the autophagy program remains unknown. We have recently discovered that a Golgi-resident protein, PAQR3, regulates autophagy initiation as it preferentially facilitates the formation of the ATG14-linked PIK3C3 complex instead of the UVRAG-associated complex. Upon glucose starvation, AMPK directly phosphorylates T32 of PAQR3, which is crucial for the activation of the ATG14-associated class III PtdIns3K. Furthermore, Paqr3-deleted mice have a deficiency in exercise-induced autophagy as well as behavioral disorders. Thus, this work not only uncovers the regulatory mechanism of PAQR3 on autophagy initiation, but also provides a potential candidate therapeutic target for neurodegenerative diseases.
刊物名称: AUTOPHAGY
英文刊物名称: AUTOPHAGY
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学科: Cell Biology
英文学科: Cell Biology
影响因子: 8.593
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论文类别: Article
英文论文类别: Article
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